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To evaluate the performance of a high-throughput research assay for HIV drug resistance testing based on whole genome next-generation sequencing (NGS) that also quantifies HIV viral load.

Plasma samples (n = 145) were obtained from HIV-positive MSM (HPTN 078). Samples were analysed using clinical assays (the ViroSeq HIV-1 Genotyping System and the Abbott RealTime HIV-1 Viral Load assay) and a research assay based on whole-genome NGS (veSEQ-HIV).

HIV protease and reverse transcriptase sequences (n = 142) and integrase sequences (n = 138) were obtained using ViroSeq. Sequences from all three regions were obtained for 100 (70.4%) of the 142 samples using veSEQ-HIV; results were obtained more frequently for samples with higher viral loads (93.5% for 93 samples with >5000 copies/mL; 50.0% for 26 samples with 1000-5000 copies/mL; 0% for 23 samples with <1000 copies/mL). For samples with results from both methods, drug resistance mutations (DRMs) were detected in 33 samples using ViroSeq and 42 samples using veSEQ-HIV (detection threshold 5.0%). Overall, 146 major DRMs were detected; 107 were detected by both methods, 37 were detected by veSEQ-HIV only (frequency range 5.0%-30.6%) and two were detected by ViroSeq only. HIV viral loads estimated by veSEQ-HIV strongly correlated with results from the Abbott RealTime Viral Load assay (R2 = 0.85; n = 142).

The NGS-based veSEQ-HIV method provided results for most samples with higher viral loads, was accurate for detecting major DRMs, and detected mutations at lower levels compared with a method based on population sequencing. The veSEQ-HIV method also provided HIV viral load data.

The NGS-based veSEQ-HIV method provided results for most samples with higher viral loads, was accurate for detecting major DRMs, and detected mutations at lower levels compared with a method based on population sequencing. The veSEQ-HIV method also provided HIV viral load data.

To determine the impact of pretreatment low-abundance HIV-1 drug-resistant variants (LA-DRVs) on virological failure (VF) among HIV-1/TB-co-infected individuals treated with NNRTI first-line ART.

We conducted a case-control study of 170 adults with HIV-1/TB co-infection. Cases had at least one viral load (VL) ≥1000 RNA copies/mL after ≥6 months on NNRTI-based ART, and controls had sustained VLs <1000 copies/mL. We sequenced plasma viruses by Sanger and MiSeq next-generation sequencing (NGS). We assessed drug resistance mutations (DRMs) using the Stanford drug resistance database, and analysed NGS data for DRMs at ≥20%, 10%, 5% and 2% thresholds. https://www.selleckchem.com/products/nst-628.html We assessed the effect of pretreatment drug resistance (PDR) on VF.

We analysed sequences from 45 cases and 125 controls. Overall prevalence of PDR detected at a ≥20% threshold was 4.7% (8/170) and was higher in cases than in controls (8.9% versus 3.2%), P = 0.210. Participants with PDR at ≥20% had almost 4-fold higher odds of VF (adjusted OR 3.7, 95% CI 0.8-ons.

To investigate resistance-associated substitutions (RASs) as well as retreatment efficacies in a large cohort of European patients with failure of glecaprevir/pibrentasvir.

Patients were identified from three European Resistance Reference centres in Spain, Italy and Germany. Sequencing of NS3, NS5A and NS5B was conducted and substitutions associated with resistance to direct antiviral agents were analysed. Clinical and virological parameters were documented retrospectively and retreatment efficacies were evaluated.

We evaluated 90 glecaprevir/pibrentasvir failures [3a (n = 36), 1a (n = 23), 2a/2c (n = 20), 1b (n = 10) and 4d (n = 1)]. Ten patients were cirrhotic, two had previous exposure to PEG-interferon and seven were coinfected with HIV; 80 had been treated for 8 weeks. Overall, 31 patients (34.4%) failed glecaprevir/pibrentasvir without any NS3 or NS5A RASs, 62.4% (53/85) showed RASs in NS5A, 15.6% (13/83) in NS3 and 10% (9/90) in both NS5A and NS3. Infection with HCV genotypes 1a and 3a was associeatment of glecaprevir/pibrentasvir failures with sofosbuvir/velpatasvir/voxilaprevir achieved viral suppression across all genotypes.Berry syndrome is a rare congenital cardiac lesion consisting of a distal aortopulmonary window, the aortic origin of the right pulmonary artery (PA), intact ventricular septum and an interrupted or hypoplastic aortic arch. Different repair techniques have been described in the literature. We report a case of Berry syndrome, in whom myocardial ischaemia developed following direct implantation of the right PA to the main PA, which was resolved using an interposition tube graft.

Does oxygen concentration during 3-day embryo culture affect obstetric and neonatal outcomes?

Oxygen concentration during 3-day embryo culture does not seem to affect the obstetric and neonatal outcomes measured.

Atmospheric oxygen appears to be harmful during extended embryo culture. Embryo culture conditions might therefore be a potential risk factor for subsequent fetal development and the health of future children. No data are available concerning the obstetrics and neonatal outcomes after Day 3 transfer of embryos cultured under reduced and atmospheric oxygen tensions.

A secondary analysis of a previous randomized controlled trial assessing clinical pregnancy outcomes was carried out. This analysis included 1125 consecutive oocyte donation cycles utilizing ICSI or IVF and Day 3 embryo transfers between November 2009 and April 2012. The whole cohort of donated oocytes from patients who agreed to participate in the study were randomly allocated (11 ratio) to a reduced O2 tension group (6% O2) or anhermore, long-term studies investigating the effect of using atmospheric O2 are also needed. Gathering these type of clinical data is indeed, quite relevant from the safety perspective. The present data show that, at least in egg donation cycles undergoing Day 3 embryo transfers, culturing embryos under atmospheric oxygen concentration seems not to affect perinatal outcomes.

The present project was supported by the R + D program of the Regional Valencian Government, Spain (IMPIVA IMDTF/2011/214). The authors declare that they have no conflict of interest with respect to the content of this manuscript.

NCT01532193.

NCT01532193.

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